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The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.

Al's Comment:

There has been predjuduce against marijuana as a treatment for cancer simply because in most states it is illegal.  Removing the psychoactive components should immediately remove that barrier.


Posted on: 04/29/2015

  J Neuroimmune Pharmacol. 2015 Apr 28. [Epub ahead of print]
The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.
McAllister SD1, Soroceanu L, Desprez PY.
 
Author information:
1California Pacific Medical Center Research Institute, 475 Brannan Street, Suite 220, San Francisco, CA, 94107, USA, mcallis@cpmcri.org.
 
Abstract
 
As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ9-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes. Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy. During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers. In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors. For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer. This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells. We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.
PMID: 25916739 [PubMed - as supplied by publisher]

 


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